Prostacyclin production by arterialized autogenous venous grafts in dogs.
Arteries are capable of producing significantly larger quantities of prostacyclin than are veins. To test the hypothesis, whether prostacyclin production by the vessel wall is related to blood pressure and flow, we measured the amounts of PGI2 released and synthesized by venous segments transplanted for 6 weeks into the arterial circulation. These results were compared with the production of prostacyclin by normal veins and arteries. In 20 dogs a segment of jugular vein was interposed into the carotid system; a sham dissection was done on the opposite side. "Arterialized" vein grafts showed prominent intima lined by endothelium, medial smooth muscle cell proliferation and fibrotic proliferation in adventitia. Spontaneous and arachidonic acid-stimulated prostacyclin production (measured by radioimmunoassay for 6-keto-PGF1 alpha) was not significantly different between arterialized venous autografts and jugular veins. Significantly larger amounts of prostacyclin were synthesized by the carotid artery. Thus, histologic changes and rheologic effects occurring in vein grafts transposed to the arterial site do not affect prostacyclin production.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D001158:Arteries / Q000033:anatomy & histology / Q000378:metabolism*; D001161:Arteriosclerosis / Q000209:etiology; D001794:Blood Pressure; D004285:Dogs; D011464:Epoprostenol / Q000096:biosynthesis*; D011453:Prostaglandins / Q000096:biosynthesis*; D012039:Regional Blood Flow; D014680:Veins / Q000033:anatomy & histology / Q000378:metabolism* / Q000637:transplantation
D001095:Arachidonic Acids; D011453:Prostaglandins; D016718:Arachidonic Acid; D011464:Epoprostenol